Aging-Related Degeneration Can Be Caused by Defects of Energy Metabolism in Tissue Stem Cells

The results are a breakthrough in revealing the unexpected importance of energy metabolism in regulating stem cell function and tissue maintenance. These findings increase the understanding of mechanisms of aging-related degeneration.

The findings of the researchers at the University of Helsinki, Finland, increase the understanding of mechanisms of aging-related degeneration. The results are a breakthrough in revealing the unexpected importance of energy metabolism in regulating stem cell function and tissue maintenance.

Aging-related tissue degeneration can be caused by mitochondrial dysfunction in tissue stem cells. The research group of Professor Anu Suomalainen Wartiovaara at the University of Helsinki, with their collaborators in Max Planck Institute for Biology of Aging, Karolinska Institutet, and University of Wisconsin, reported their results on mechanisms of aging-associated degeneration.

Stem cells are called the spare parts for tissues, as they maintain and repair tissues during life. They are multipotent and can produce a variety of different cell types, from blood cells to neurons and skin cells. Mitochondria are the cellular engine: they transform the energy of nutrients to a form that cells can use, and in this process they burn most of the inhaled oxygen. If this nutrient ‘burning’ is inefficient, the engine will produce exhaust fumes, oxygen radicals, which damage cellular structures, including the genome. Antioxidants target to scavenge these radicals.

Already in 2004 and 2005 a research model was created in Sweden and USA, which accumulated a heavy load of mitochondrial genome defects. This led to symptoms of premature aging: thin skin, graying of hair, baldness, osteoporosis, and anemia.

In the current publication, scientist Kati Ahlqvist in Professor Suomalainen Wartiovaara’s group showed that these symptoms were partially explained by stem cell dysfunction. The number of stem cells did not reduce, but their function was modified: the progeny cells in blood and the nervous system were dysfunctional. The researchers also found out that these defects could be partially prevented by early antioxidant treatment.

“This suggests that oxygen radicals can regulate stem cell function and that these cells are very susceptible for mitochondrial dysfunction. These findings may also be important to understand mechanisms of mitochondrial disease,” Professor Suomalainen Wartiovaara (pictured), says.

The results are a breakthrough in revealing the unexpected importance of energy metabolism in regulating stem cell function and tissue maintenance. These findings increase the understanding of mechanisms of aging-related degeneration.